Latest Research Papers
To Die or Not to Die: How Sublethal Damage Rewires Cell Fate and Implications for Sepsis.
Lytic cell death has long been regarded as an irreversible process culminating in plasma membrane rupture. However, accumulating evidence indicates that the activation of lytic pathways does not invariably result in cell lysis. Instead, cells can undergo sublethal membrane damage, a state in which membrane injury is limited, allowing cells…
Crosstalk of regulated cell death pathways in sepsis-associated acute kidney injury: implications for therapy.
Sepsis-associated acute kidney injury (SA-AKI) is a common and severe complication in critically ill patients, independently associated with significantly increased mortality and a high risk of progression to chronic kidney disease. The pathogenesis of SA-AKI is complex and involves not only traditional concepts such as renal hypoperfusion, microcirculatory dysfunction, and…
Modulation of the cytoskeleton for cancer therapy.
All degenerative diseases are associated with impairment in intracellular trafficking. The highly dynamic organization and remodeling of the cellular cytoskeleton are dysfunctional in pathology and often lead to drug resistance. Successful analyses of the mechanisms of drug action require statistical analysis of large-scale readouts of molecular interactions at nanometer-scale resolution.…
Neurotoxic mechanisms of cadmium in neurodegenerative diseases.
Cadmium (Cd) is a highly toxic, bioaccumulative heavy metal increasingly implicated in the pathogenesis of neurodegenerative disorders. This review systemically characterizes the molecular mechanisms underlying Cd-induced neurotoxicity, with particular emphasis on oxidative stress-mediated pathways that initiate interconnected processes including ferroptosis, mitochondrial impairment, disruption of calcium homeostasis, and chronic neuroinflammation. Evidence…
Spatiotemporally programmed hybrid nano-prodrugs orchestrate multidimensionally synergistic cascade lethality in NSCLC.
Non-small cell lung cancer (NSCLC) develops a high GSH/GPX4 antioxidant phenotype under persistent oxidative pressure, which suppresses membrane lipid peroxidation and ferroptosis, constituting a core mechanism underlying chemotherapy resistance and suboptimal therapeutic efficacy. Breaking this resistance barrier demands not simply attacking the tumor but disarming the antioxidant defense to intensify…
Ferroptosis-driven stromal immune evasion and melatonin receptor suppression as novel predictive biomarkers of immunotherapy response in oral squamous cell carcinoma: a single-cell transcriptomic study.
Immune checkpoint inhibitor (ICI) therapy for oral squamous cell carcinoma (OSCC) yields objective responses in fewer than 20% of patients, underscoring the urgent need for novel predictive biomarkers beyond PD-L1 expression and tumor mutational burden (TMB). Ferroptosis, an iron-dependent oxidative cell death program, has emerged as a dual-function regulator of…
Engineered nanomedicine remodels the postoperative cavity microenvironment to suppress glioblastoma recurrence.
Glioblastoma (GBM) has a high rate of post-surgical recurrence, which can be attributed to residual tumor cells as well as to the disruption of the tumor microenvironment (TME) caused by surgery. Here, we define the postoperative cavity microenvironment (POCM) as a pathological niche with distinct spatial and temporal boundaries, and…
α-ketoglutarate ameliorates spinal motor neuron ferroptosis after sacral plexus transection via enhancing PINK1 O‑GlcNAcylation and mitophagy.
Sacral plexus transection (SPT), mostly caused by high‑energy trauma, induces secondary death of spinal motor neurons in the lumbosacral segments and contributes to poor clinical outcomes after nerve repair. This study aimed to investigate the protective effect of α‑ketoglutarate (AKG) against ferroptosis in spinal motor neurons following SPT and the…
Reversible Imaging of the HOCl/GSH Redox Cycle Reveals the HOCl-Ferroptosis Regulatory Axis in Ischemic Stroke.
Ferroptosis has emerged as a significant contributor to ischemia-reperfusion injury after ischemic stroke; however, the redox events linking oxidative stress to ferroptotic injury remain poorly understood. To this end, we developed DX, a fluorescent probe targeting lipid droplets and capable of reversibly tracking the HOCl/GSH redox cycle in living systems.…
Hydrogen Sulfide Suppresses RANKL-Induced Osteoclast Differentiation by Modulating Nrf2/GPX4 Signaling.
Excessive osteoclast activity drives bone-resorptive disorders, and oxidative stress is a key regulator of osteoclast differentiation. Hydrogen sulfide (H?S), an endogenous antioxidant, may modulate this process, but its mechanisms remain unclear. In this study, RANKL (50 ng/mL) was used to induce osteoclastogenesis in RAW264.7 cells, with or without the H?S…